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Am J Physiol Regul Integr Comp Physiol (July 20, 2006). doi:10.1152/ajpregu.00353.2006
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Submitted on May 25, 2006
Accepted on July 17, 2006

Impact of androgen-induced oxidative stress on hypertension in male SHR

Radu Iliescu1, Valeria E Cucchiarelli1, Licy L. Yanes1, Joshua W. Iles1, and Jane F. Reckelhoff1*

1 Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi, United States

* To whom correspondence should be addressed. E-mail: jreckelhoff{at}physiology.umsmed.edu.

Men have higher blood pressure than women, and androgens and oxidative stress have been implicated as playing roles in this sexual dimorphism. The SHR is an animal model of both androgen- and oxidative stress-mediated hypertension. Therefore, the present studies were performed to test the hypothesis that androgens cause hypertension in SHR in part by stimulating superoxide production via NADPH oxidase. Castration of male SHR reduced blood pressure by 15% and attenuated both basal and NADPH-stimulated superoxide production in kidney cortical homogenates. Expression of p47phox and gp91phox but not p22phox subunits of NADPH oxidase were significantly lower in kidney cortex from castrated males compared to intact males. Moreover, inhibition of NADPH oxidase with apocynin caused approximately 15 mm Hg reduction in blood pressure and reduced basal and NADPH-stimulated superoxide production in intact male SHR, but had no effect on blood pressure or superoxide production in castrated males. These data support the hypothesis that androgens cause oxidative stress and thereby increase blood pressure in male SHR via an NADPH oxidase-dependent mechanism.




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